Sharing some raw data and thoughts on the LUCAS, ITD, CPR and Epi from my lab

I don’t know of too many researchers that share raw data directly from their lab. Dr. Jeffrey Kline however seems to be setting a pretty good example of a leading researcher in a field interacting directly with the masses, which I think is an excellent thing. Now I have no delusions that I am anywhere near the stature of Dr. Kline, in fact part of the reason I’d like to share some of my data through my blog is that as a full time med student and part time researcher, it feels like it’s going to take me forever to get all this stuff collected and into a publishable quality. Even though we are not done collecting data, and the differences seen now may eventually fade into statistical obscurity, there are still things I get to see first hand doing my research that are flat out amazing to me. And I’d like to share some of those with you here.

First I’m going to share one of my carotid blood flow strips with some notations on it so you can see some data yourself. Study this for a minute and then I’ll go over some of my thoughts on it and the lab in general below.

The LUCAS doesn’t take very long to place. Sure it takes longer to put on than it does to start manual CPR. It also takes a little longer to place on my pigs since they have a larger anterior-posterior diameter than humans it requires placing them in the LUCAS rig along with a V-shaped wedge and some towels so they don’t roll onto their side (which is why vets do CPR on the animals side). Also I’m not rushing when I place it, I don’t measure this as one of my data points in this study, so 53 seconds is me at my leisure! I’m literally coming off the chest, walking across the room, unplugging the LUCAS from the wall charger, walking back to the pig and placing it. When using it on humans, after some practice, I felt the time to place was quite short and someone was always doing manual CPR while getting the machine ready so I don’t personally feel this is that big of an issue. Especially since…

The LUCAS does more consistent CPR than a human is capable of. This is not to say outcomes are different, this is not to say it produces more blood flow (it doesn’t), but it is plainly obvious that the LUCAS does more consistent CPR than a human is physically capable of doing. It’s a machine, so of course it will. Comparatively human CPR quality is all over the place. In this one data set human CPR spent 45.5 seconds under 25% of baseline carotid blood flow. That’s almost 10% of the time! And this is in a research setting, not moving from house to ambulance to ED. The LUCAS on the other hand, after placement, spent 0% of the time under 25%.

Human CPR is capable of producing more blood flow than the LUCAS. But it’s very difficult to get this to be consistent. There are days when the average on the LUCAS wins and days when the human wins. That’s the funny part about trying to research something as inconsistent as manual CPR. This is why I think the pit-crew CPR approach works. It puts training and emphasis on good CPR. So in a short, 10-20 minute arrest, it is likely the humans would only start to lose to the LUCAS towards the end. Where the LUCAS shines is anything past that, it allows you to go beyond human limits and do so without physically fatiguing your crew. If someone thinks otherwise (friendly poke @DrHowieMell 😉 ) then I would be happy to host your best team in my lab and see how they performed against a LUCAS.

The longer you do CPR without interruption, the more blood flow you get. I know this is well known, but this is for real. I see a “ramp up” effect every time I do this lab. Better, longer CPR, especially with the LUCAS continues to climb in carotid blood flow (and ETCO2 for that matter).

The effect of the ITD (Impedance Threshold Device aka ResQPod) is difficult to see. I’ve liked the ITD for a long time but when I got the ability to see carotid blood flow, the difference is there but it’s smaller than I expected from ETCO2 data. It’s always changed ETCO2 (a surrogate marker for flow) but there has always been concern that the change in airway physiology could be to blame for this. It appears there may be a difference in VCO2 (volumetric ETCO2, a way to account for changes in minute volume to better view CO2 production and perfusion) but the effect so far has not been statistically significant. I still like it, I haven’t seen anything to say it’s bad, but I can’t personally give you data from my lab that firmly supports it yet.

Abdominal binding seems to be helpful. This is something that Dr. Lurie and Yannopolous have been doing for a while. That’s not displayed in this data set but in the last lab I did I tried adding some abdominal pressure and average carotid blood flow increased by about 7%. We will be trying this out more in the future.

Epinephrine is awful. Seriously, at a 1 mg dose epinephrine is straight poison as far as I’m concerned. I’ve proved it at the cellular and organ level with my rat heart model (you’ll see more about this on this blog later) and I’m proving it now with my pig model. It kills ETCO2 as well which is a marker for poor perfusion as well as carotid blood flow which is a measure of poor blood flow. There may be a role of epinephrine in arrest at the push-dose-pressure dosage or something like this, but at the 1mg empiric therapy this needs to go away. The effect seen perfectly explains how epinephrine increases vascular resistance, which increases those easy to measure pressures making us feel all warm and fuzzy. All the while we’re decreasing the only important things flow and subsequently perfusion. This is why epinephrine increases ROSC without increasing survival, you’re actually making the perfusion of the brain worse when you give it. I’ve seen this in my rat model, when you restore perfusion ROSC will happen on its own without epinephrine, it just takes a little longer (more ammo for the ECLS argument).

As a disclaimer, I’m not here to debate animal rights but I feel this needs to be addressed. I understand animal research is contentious and I can even empathise with animal rights champion’s concerns. I will tell you that everything we are doing is legal, approved by an animal use and ethics committee and follows all applicable standards and guidelines. I will also tell you that when I started doing this I was an experienced paramedic but had no experience with animal labs so I treated my pigs the same way I treated my human patients anesthesia wise. Which after spending time in other animal labs and rotating through the ICU, my pigs actually get more anesthesia than you would in the either the university animal labs I’ve seen or an ICU. I’ve unfortunately actually lost animals due to too much sedation and while tragic and far from ideal I would rather have that than them waking up in pain. We use multiple concurrent study protocols and employ student teaching/training during our labs which makes the most use out of every animal. The data and training coming from this lab directly impacts human patient care. So for anyone with concerns about the animal research component, you have the right to think what I’m doing is wrong. Just know that I am an animal lover too, these pigs are my babies; their sacrifice does not take place without the dignity and honor it deserves and in no way do they suffer.

13 thoughts on “Sharing some raw data and thoughts on the LUCAS, ITD, CPR and Epi from my lab”

This is amazig and thank you for sharing your data with everyone!
One question: how do you measure carotid flow?? I am from a system, where use radial art lines to guide CPR (in OHCA) instead of etCO2 as we found massive AaCO2 differences and belive that it could give you a false security about your CPR quality. None the less, sys BP is not equivalent to flow!
Thx again Marcel

Thanks Marcel! Carotid blood flow is measured by a surgically placed duplex ultrasound probe so not something that could be done clinically. We also measure arterial blood pressure, ETCO2, VCO2, PeCO2 and more. We have found in our lab that ETCO2 is the best marker of perfusion, ironically SYS BP has shown to at times have an INVERSE relationship with flow, so in our experience it is not only useless as a marker of perfusion but can easily be misleading and this was without epinephrine usage, once you start giving epinephrine the blood pressure is meaningless. A perfect system for measuring perfusion has been created but is not commonly in use. It consists of measuring Transcutaneous CO2 and ETCO2 to show a perfusion deficit when the two separate. This is not commonly available clinically however and I have little first hand knowledge of the TCO2 system but I know it’s definitely not fool proof. So while we wait for that system to develop out I think the next best flow marker would probably be VCO2. But I definitely dislike pressure as a marker of flow. Best of luck to you and thanks for reading!

Re-reading your comment, you’re saying massive arterial to alveolar CO2 differences? If so this is similar concept to the TCO2 vs ETCO2 differences. Yes this would show poor perfusion but I think would more likely be attributable to down times, epinephrine use etc, I would doubt this could be done real time enough to gauge CPR quality but I’m interested to hear more about your experiences if possible!

Your thought on application of mechanical CPR after 10-20 minutes of CPR is intriguing from a purchasing and deployment stand point.

My thought….A system with limited resources might have similar success putting a single or low number of mechanical CPR devices on supervisor or battalion chief response vehicle compared to a system that puts a mechanical CPR device on every ambulance.

This is how many services use mechanical CPR. Even if you have MCPR on every box you will still be doing manual CPR for a few minutes while getting the machine and applying it. My important finding to me was that manual CPR can be better if you do it well, but there is just no way to do it like that continuously. Plus it’s a huge mental drain. Once you place patient on MCPR you can sit back and think and don’t have the compressor change delay every 2 mins either. Plus easier to move patient on MCPR.

I am not sure how you would do this in your lab, but it would be fascinating to do push dose Epi dose based soley on ETCO2 drops, not on an arbitrary time interval.

I am 100% in agreement with you on the Lucas as well. We have always had ROSC rates above 30% , but we are currently in the 45-49% range for VF/VT and in the 20-30% range for other arrests as well, since we have addopted tennets fo high performance CPR. We do put the lucas on earlyier than 10-20 minutes (in too stages thogh to reduce inturruptions), and have had several patients wake up with compressions and in VF. Thats a pretty strong indicator of cerebral perfusion if you ask me, lab or no lab.

the other shift we have had is using ETCO2, not an arbitrary time ..to gauge termination of arrest. if ETCO2 stays up, I will transport even a PEA or asystolic arrest..IF ETCO2 is good. To this end we have had several case studies for good outcomes with good CPC scores, not just ROSC in the ER. In this the LUCAS truely rocks, as it takes away the crappy BS CPR periods going down halways or gurney surfing bull crap.

Thank you for posting this! For years I’ve been wishing that someone would share their animal model resuscitation experiences online because there’s not too much out there that’s easily accessible outside of the journals (and who wants to slog through those if they’re not actively researching a topic). Can’t wait to see what else you gentlemen have in store for us.

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